Faculty > Huang

Andrew J.W. Huang, M.D., M.P.H.

Professor of Ophthalmology and Visual Sciences
Lab: (314)362-0622, Fax: (314)362-0627

M.D. National Taiwan University School of Medicine, Taipei, Taiwan (1974-1981);
M.P.H. Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD (1981-82);
Postdoctoral Fellow, Division of Biophysics, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD (1982-1984);
Research Fellow in Ophthalmology, Harvard Medical School, Boston, MA (1984-1986);
Resident in Ophthalmology, Bascom Palmer Eye Institute, University of Miami, Miami, FL (1987-1990);
Clinical Fellow in Cornea and External Disease, Bascom Palmer Eye Institute, University of Miami, Miami, FL (1990-1991)

Research Areas:

  • Corneal epithelial wound healing
  • Corneal neovascularization
  • Corneal stromal dystrophies
  • Corneal Stem cells and Dry eye

Research Interests:

  1. Ex vivo expansion of corneolimbal stem cells for ocular surface reconstruction

    Corneal epithelial stem cells reside in limbus, a special structure located at the corneoscleral junction. Extensive ocular surface trauma or inflammation can often lead to loss of limbal stem cells, known as limbal deficiency. The hallmarks of limbal stem cell deficiency are conjunctival invasion of corneal surface, poor epithelial wound healing, corneal neovascularization and inflammation. The autologous or allogenic limbal stem cells can be cultivated and expanded in special tissue culture with various matrix carries including amniotic membrane. The expanded source may provide a viable corneal stem cell source for ocular surface rehabilitation.

  2. Molecular genetics of corneal dystrophies

    Corneal epithelial/stromal dystrophies are a group of inherited corneal conditions characterized by abnormal protein aggregations with resultant corneal opacities and recurrent epithelial breakdowns. Mutations of keratoepithelin (KE), an extracellular matrix protein also known as TGFBI or BGH3 have been identified in the affected families. KE mutations can cause either amyloid formations (such as in various types of corneal lattice dystrophy) or amorphous aggregates (such as in corneal granular dystrophy or Avellino dystrophy). The molecular basis dictating the clinical phenotype has been unclear. The KE gene is located in human chromosome 5q31 and regulated by TGF-b (transforming growth factor- beta). This lab has previously identified the KE gene promoter. However, the activating mechanism of KE gene promoter has not been delineated. Studies on the regulation of gene promoter and related KE protein expression may reveal the pathogenesis of various corneal epithelial/stromal dystrophies and facilitate the development of novel therapeutic strategies for related corneal pathology.

  3. Molecular therapy for corneal dystrophies and hereditary glaucoma

    RNA interference has been identified as a powerful tool for gene silencing. It can also be used to suppress expression of untoward genes of inherited conditions. We have developed several siRNAs (small interfering RNA containing short double-stranded RNAs) as a molecular silencer to knock down gene expression of KE and myocilin (a protein purportedly responsible for certain types of hereditary open-angle glaucoma), respectively. Using appropriate siRNA molecules, RNAi can selectively suppress the expression of KE and myocilin protein in vitro, respectively. Anterior segment of the eye is readily accessible for topical delivery of therapeutics to the target tissues such as cornea or trabecular meshwork. We are investigating the feasibility of delivering siRNAs to anterior segment as a new potential therapeutic strategy for inherited ocular conditions such as corneal dystrophies and glaucoma.

Selected publications:

  1. Wichiensin P, McDonough RL, Huang AJW, Flynn HW. Tissue adhesive in the management of leaking pars plana sclerotomy causing hypotony and choroidal detachment. Arch Ophthalmol 119:135-137, 2001.
  2. Souza PMF, Holland EJ, Huang AJW. Bilateral herpetic keratoconjunctivitis. Ophthalmology 110:493-496, 2003.
  3. Sawada Y, Fischer JL, Verm AM, Harrison AR, Yuan C, Huang AJW. Detection by impression cytology of conjunctival intraepithelial invasion from eyelid sebaceous cell carcinoma. Ophthalmology 110:2045-2050, 2003.
  4. Kobayashi A, Wajima R, Sugiyama K, Nonomura A, Huang AJW. Idiopathic limbal squamous metaplasia. Arch Ophthalmol 121:1473-1475, 2003.
  5. Sawada Y, Yuan C, Huang AJW. Impression cytology in the diagnosis of acanthamoeba keratitis with surface involvement. Am J Ophthalmol 137:323-328, 2004.
  6. Yuan C, Reuland MJ, Lee L, Huang AJW. Optimized expression and refolding of human keratoepithelin in BL21(DE3). Protein Expr Purif 35:39-45, 2004.
  7. Yuan C, Yang MC, Zins EJ, Boehlke CS, Huang AJW. Identification of the promoter region of ßIGH3 gene. Mol Vis 10:351-360, 2004.
  8. Boehm MD, Huang AJW. Treatment of recurrent corneal and conjunctival intraepithelial neoplasia with topical interferon alpha-2B. Ophthalmology 111:1755-1761, 2004.
  9. Kobayashi A, Sugiyama K, Huang AJW. In vivo confocal microscopy in the patients with central corneal cloudy dystrophy of Francois. Arch Ophthalmol 122: 1676-1679, 2004.
  10. Boehlke CS, Yuan C, Kao WWY, Huang AJW. Cytokeratin 12 in human ocular surface epithelia is the antigen reactive with a commercial anti-Gaq antibody. Mol Vis 10:867-873, 2004.
  11. Yang MC, Huang AJW. Bilateral conjunctival nodules: an unusual presentation of Vogt-Koyanagi-Harada syndrome. Arch Ophthalmol 122:1878-1881 2004.
  12. Telander D, Lee TZ, Pambuccian SE, Huang AJW. Subconjunctival corticosteroids for benign lymphoid hyperplasia. Br J Ophthalmol 89:770-771, 2005.
  13. Huang AJW, Li D-Q, Li CH, Shang TY, Hernandez E. Modulation of corneal vascularization. The Ocular Surface 3:S190-193, 2005.
  14. Yuan C, Berscheit HL, Huang AJW. Identification of an amyloidogenic region on keratoepithelin via synthetic peptides. FEBS Lett 581:241-247, 2007.
  15. Yuan C, Zins EJ, Clark AF, Huang AJW. Suppression of keratoepithelin and myocilin by small interfering RNAs (siRNA) in vitro. Mol Vis 13:2083-2095, 2007. (Role: Supervised the research projects and wrote the paper.)
  16. Huang AJW. Suppression of keratoepithelin and myocilin by small interfering RNA (an American Ophthalmological Society thesis). Trans Am Ophthalmol Soc 105:365-378, 2007.


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